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oai:repisalud.isciii.es:20.500.12105/272622026-02-23T01:19:35Zcom_20.500.12105_2327com_20.500.12105_2290col_20.500.12105_16991

00925njm 22002777a 4500 dc Jordan, Stefan author Tung, Navpreet author Casanova-Acebes, Maria author Chang, Christie author Cantoni, Claudia author Zhang, Dachuan author Wirtz, Theresa H author Naik, Shruti author Rose, Samuel A author Brocker, Chad N author Gainullina, Anastasiia author Hornburg, Daniel author Horng, Sam author Maier, Barbara B author Cravedi, Paolo author LeRoith, Derek author Gonzalez, Frank J author Meissner, Felix author Ochando, Jordi author Rahman, Adeeb author Chipuk, Jerry E author Artyomov, Maxim N author Frenette, Paul S author Piccio, Laura author Berres, Marie-Luise author Gallagher, Emily J author Merad, Miriam author 2019-08-22 Caloric restriction is known to improve inflammatory and autoimmune diseases. However, the mechanisms by which reduced caloric intake modulates inflammation are poorly understood. Here we show that short-term fasting reduced monocyte metabolic and inflammatory activity and drastically reduced the number of circulating monocytes. Regulation of peripheral monocyte numbers was dependent on dietary glucose and protein levels. Specifically, we found that activation of the low-energy sensor 5'-AMP-activated protein kinase (AMPK) in hepatocytes and suppression of systemic CCL2 production by peroxisome proliferator-activator receptor alpha (PPARα) reduced monocyte mobilization from the bone marrow. Importantly, we show that fasting improves chronic inflammatory diseases without compromising monocyte emergency mobilization during acute infectious inflammation and tissue repair. These results reveal that caloric intake and liver energy sensors dictate the blood and tissue immune tone and link dietary habits to inflammatory disease outcome. Cell . 2019 Aug 22;178(5):1102-1114. Cell 31442403 https://hdl.handle.net/20.500.12105/27262 AMPK CCL2 Caloric restriction PPARα fasting inflammation inflammatory disease liver metabolism monocyte Dietary Intake Regulates the Circulating Inflammatory Monocyte Pool.